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*Department of Anesthesiology, Institute of Clinical Medicine, and
Department of Biomedical Engineering, Institute of Basic Medical Science, University of Tsukuba, Tsukuba, Japan; and
Department of Anesthesiology and Intensive Care, Hamamatsu University School of Medicine, Hamamatsu, Japan
Address correspondence and reprint requests to Masayuki Miyabe, MD, Department of Anesthesiology, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Japan, 305-8576. Address e-mail to miyabe{at}igaku.md.tsukuba.ac.jp
The adhesion of polymorphonuclear leukocytes to the capillary endothelium is one of the key events in the pathophysiology of hemorrhagic shock. We studied sodium nitroprusside (SNP) for its ability to modulate leukocyte-endothelial cell interactions induced by hemorrhagic shock and reinfusion of blood by using intravital microscopy of the rat mesentery. Administration of SNP at a dose of 0.1 µg · kg-1 · min-1 infusion neither significantly decreased mean arterial blood pressure nor significantly altered bleedout volumes in hemorrhagic rats, indicating that SNP at this dose did not modify the severity of the shock protocol. Resuscitation from 1 h of hemorrhagic shock (mean arterial blood pressure approximately 45 mm Hg) significantly increased the number of adherent and emigrated leukocytes in the rat mesenteric microcirculation. However, infusion of SNP, started 15 min before hemorrhage, and continued over the entire experimental period, markedly reduced the leukocyte adhesion after reinfusion and emigration during hemorrhagic shock and after reinfusion. We concluded that the nitric oxide donor SNP is effective at reducing the leukocyte-endothelial interaction after blood reinfusion after hemorrhagic shock in rats.
IMPLICATIONS: The IV infusion of 0.1 µg · kg-1 · min-1 of sodium nitroprusside, a dose that does not exert a significant vasodilator effect, reduces leukocyte adhesion and emigration after hemorrhagic shock.
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